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3154 MSK > OA > Flashcards

OA Flashcards

1
Q

OA definition

A
  • Degenerative disease (with inflammation) of bone & joint cartilage
    • Add on to the pre-existing wear and tear
    • Impaired repairing process of joints
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2
Q

cases

A
  • Wear and tear
  • Not inflammatory initially
  • Pain grows with use (more damage)
  • Degenerative joint disease
  • Progressive and irreversible loss of cartilage
  • Most common inflammatory joint disorder
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3
Q

patho of OA

A

1) Articular cartilage damage
2) Chondrocyte activity (To remove and repair damage)
3) Aberrant chondrocyte – incr breakdown of cartilage
4) Apoptosis of chondrocyte
a. Cartilage loss
b. Subchondral bone release of vasoactive peptides & MMP (more collagen break down)

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4
Q

effect of chondrocyte apoptosis

A
  • production of collagen and the extracellular matrix

5) Formation of fibrillation (cracks) in cartilage & cartilage shards
a. inflammation in joint capsule and synovium
b. effusion and synovial thickening
c. pain (nerve endings in joint)

6) subchondral bones rub against each other
a. smooth (eburnation), brittle
b. decr weight bearing ability

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5
Q

inflammatory – > compensatory response

A

1) Cartilage degradation (joint space narrow)

2) Bone remodeling (sclerosis, osteocytes)

3) Synovial inflamm

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6
Q

cartilage degradation

A

a. Articular cartilage damage –> chondrocytes proliferate, phenotypic switch
b. Produce improper mineralised collagen
c. Weaken and degradation of collagen matrix in synovium

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7
Q

Bone remodeling (sclerosis, osteocytes)

A
  • Weakened collagen matrix –> thickening of subchondral bones
    i. Sclerosis
    ii. Osteophytes, bone spurs
  • Widen joints to try to stabilise
  • Response to abnormal mechanical loads
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8
Q

synovial inflam

A

a. Weaken and degradation of collagen matrix –> cartilage flakes off (shards)
b. Lymphocytes and macrophages recruited by synovial mem (Remove debris)
c. Proinflamm cytokines produced
d. Synovitis (inflamm)

  • Disease progression. More proinflamm cytokines & DAMPs (damage-associated molecular patterns)
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9
Q

features of OA

A
  • Sclerosis (thickening of bone)
  • Microfractures
  • Osteophytes (compensatory struc to stabilise OA joints)
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10
Q

risk factors

A
  • Genetic predisposition
    • Mutation in collagen types II, IX, XI, GDF-5
  • Anatomic factors
    • Misalignment
      ○ Bow-legged, knocked knees
  • Joint injuries
    • Sports, surgery
  • Obesity
    • Load on weight-bearing joints
    • Metabolic OA
  • Aging
    • Change in ECM: thin, brittleness, dehydration
  • Gender, occupation
    • Activities, stress on knee
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11
Q

presentation of OA

A
  • pain
  • swelling (joint effusion w/ severity)
  • erythematous, warm
  • Morning stiffness < 30mins
    • Resolves with motion
    • Recurs with rest
    • Worsens with joint use (late afternoon/ night pain)
  • Limited joint movements
  • Functional limitation/ instability
  • Asymmetrical polyarthritis (weight-bearing joints)
    • Hand, knee, hip
      • Depend on factors that triggered (trauma)
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12
Q

OA pain stage

A
  • Insidious onset (slow progression over yrs)
  • Worse with joint use, relieved by rest
    ○ Going down stairs/ slope
    ○ Most severe over joint line
  • Assoc w/: ANX, DEP, sleep disturbances

stage 1: predictable sharp pain with insult (modest effect on function)
stage 2: constant pain, unpredictable stiffness (daily activity affected)
stage 3: constant dull/ ache pain. ep of intense unpredicted pain (severe limit function)

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13
Q

physical exam of OA

A
  • Asymmetric monoarticular or oligoarticular
  • Crepitus on motion (air, cartilage shards)
  • Reduced range of motion
  • Transient joint effusion (incr w/ severity)
  • Palpable warmth
  • Bone tenderness
  • Bone enlargement (fingertips: node)
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14
Q

radiographic exam and lab exam

A

Radiographic (mostly in ADVANCED STAGE)
- Joint space narrowing
- Marginal osteophytes
- Subchondral bone sclerosis
- Abnormal alignment of joint.

Lab
- ESR < 20mm/h (no inflamm)

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15
Q

dx of OA

A
  • Diagnosed w/ or w/o radiography or lab investigations in presence of typical s&sx (at risk grp)
    * Radiographic changes may not be observed until severe (joint space, sclerosis, spurs)
    * dx w/o imaging for (>45yo, activity related joint pain, morning stiff <30mins)
  • additional test for (younger indiv/ atypical s&sx)
    * hx of recent trauma, rapid worsen/ deformity, infeciton/ malignancy/ red flags
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16
Q

investigation for differentials dx

A
  • May need joint aspiration (synovial fluid)
  • Crystals, WBC
    ○ Gout? Septic arthritis?
  • RF, anti-CCP
    ○ RA
  • ESR, CRP
    ○ Inflammatory markers
  • Imaging
    ○ Extent of damage
    ○ Early disease may not be visible (But to have a baseline)
  • Evaluate tx outcomes
17
Q

tx plan

A

1) pain relief (inflammation if any)
2) improve/ preserve range of motion (non-pharm)
3) QOL

18
Q

pain relief using

A

1) analgesics (TOP –> PO)
2) slow acting (IA CS)
3) Others - duloxetine, capsaicin

19
Q

1) pain relief, anti-inflam

A
  • Paracetamol
  • Non-selective NSAIDs (diclofenac)
    ○ Accumulates in joint, longer t1/2 (less GI ADR + better analgesic effects)
    ○ Topical –> PO
  • COX2i (celecoxib)
  • Corticosteroids
20
Q

NSAIDS consideration

A

1) Topical NSAIDs (esp for knee)
a. Diclofenac gel, ketoprofen plaster
b. Considerations: hand (washing), deep joints (hip)

2) Oral (NSAIDs/ coxibs)
a. Considerations: GI, CVS, renal toxicity, AERD,
b. Lowest effective dose, PRN
c. +/- PPI/ change to COXIBS

21
Q

other analgesics

A
  • paracetamol (ST, mod-severe, NSAID CI)
  • tramadol (ST, mod-severe, constipation)
  • duloxetine (SNRI, mod-severe, CI/ Fail NSAID)
    * 5HT3 (GI, sexual), hypoNa, bleed risk, EPSE
  • top capsaicin
    * agonist for TRPV1 expressed on nociceptive nerve fibers. initial enhance pain –> defunctionalisation and reduce TRPV1)
    * TOP site rxn (burn, erythema, pain)
22
Q

2) sx slow acting drug

A

Intra-articular hyaluronic acid
* Large glycosaminoglycan (naturally found in synovial fluid)
○ Shock absorber
○ Traumatic energy dissipation
○ Protective coating of cartilage
○ Lubrication
○ Reduce pain & stiffness
* Induce biosynthesis of HA & ECM

23
Q

IA CS duration & CI

A
  • ST sx relief (4-6wk relief). Mod-severe pain, CI/ fail with NSAIDs
    ○ No LT benefit w/ regular use
  • <3 inj/ yr (4mnths)
  • CI: periarticular infection/ septic arthritis/ periarticular fracture, joint instability, juxtaarticular osteoporosis
    # risk due to effect on osteoblasts & osteoclast
24
Q

3) suppl

A

Chondroitin sulphate, glucosamine supplements

  • Inadequate or inconsistent evidence
25
Q

non pharm

A
  • Exercise
    • Reduce pain
    • Improve physical function
      ○ Incr strength of muscles supporting joints
      ○ Improve joint stability
    • Preserve joint function (strengthening exercise, neuromuscular training, low-impact aerobic, mind-body )
      ○ 30min, 3x/wk
      ○ Adherence for LT benefits.
  • Self-efficacy & self-management
  • Weight loss
    • Improve QOL, physical function
    • Reduce pain (load on weight-bearing joints, adipokines-related inflamm)
  • Supportive devices: cane, knee brace
26
Q

referral for OA

A
  • For surgical tx
  • Total joint arthroplasty (replacement)
    • Last 10-15yrs
    • Postop rehabilitation for successful outcome
      ○ Physiotherapy
      ○ Analgesics
  • CI:
    • Active infection (preop assessment, ESR, CRP, joint aspiration, MRI)
      ○ Chronic lower extremity ischemia
      ○ Skeletal immaturity

3154 MSK (9 decks)

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